Role of the complement‐lectin pathway in anaphylactoid reaction induced with lipopolysaccharide in mice

Świerzko, Anna St.; Cedzyński, Maciej; Kirikae, Teruo; Nakano, Masayasu; Klink, Magdalena; Kirikae, Fumiko; Ziółkowski, Andrzej; Vinogradov, Evgeny; Kawakami, Michiyuki

doi:10.1002/eji.200323949

Cited by 16 publications

(14 citation statements)

References 38 publications

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“…Although the most effective LPS ligands of MBL are mannosecontaining OPS as in the case of K. pneumoniae O:3, Escherichia coli O:8 and O:9, interaction of MBL with the core oligosaccharide may lead to serious biological consequences (early-phase endotoxic shock, death) as was demonstrated by Swierzko et al (2003) in a murine model. A Ra chemotype LPS-reactive factor was identified and later recognized as MBL that interacted with Ra-chemotype Salmonella LPS resulting in complement activation (Ihara et al, 1982(Ihara et al, , 1991Ji et al, 1988Ji et al, , 1993Matsushita et al, 1992).…”

Section: Discussionmentioning

confidence: 94%

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Interaction of human mannose-binding lectin (MBL) with Yersinia enterocolitica lipopolysaccharide

Kasperkiewicz

Swierzko

Bartłomiejczyk

et al. 2015

International Journal of Medical Microbiology

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Section: Discussionmentioning

confidence: 94%

“…The IC octasaccharide is truncated by 4, 5 or 6 sugar residues, respectively. core oligosaccharides of some other bacteria (Jiang et al, 1995;Swierzko et al, 2003;Dumestre-Perard et al, 2007). MBL belongs to the collectin family: a group of Ca 2+ -dependent lectins possessing a collagen-like helical domain.…”

Section: Introductionmentioning

confidence: 99%

Interaction of human mannose-binding lectin (MBL) with Yersinia enterocolitica lipopolysaccharide

Kasperkiewicz

Swierzko

Bartłomiejczyk

et al. 2015

International Journal of Medical Microbiology

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“…It binds to CD14 and/or CD11b/CD18 at the cell surface and facilitates an interaction with Toll-like receptor 4-MD complex, which via signal transduction cascades ultimately leads to activation of transcription factors (51). The interplay between LPS and complement is complex (52,53). A possible effect of LPS in the meconium-induced inflammatory reaction should be considered.…”

Section: Discussionmentioning

confidence: 99%

Complement C5a Is a Key Mediator of Meconium-Induced Neutrophil Activation

Castellheim

Pharo

Fung³

et al. 2005

Pediatr Res

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Meconium aspiration syndrome is a serious condition of the newborn characterized by pulmonary inflammation with substantial neutrophil infiltration. We recently showed that meconium is a potent activator of complement. The aim of the present study was to investigate a possible role for complement in meconiuminduced neutrophil activation. Meconium was incubated in human whole blood anticoagulated with lepirudin, a specific thrombin inhibitor that does not affect complement activation. Complement activation was detected by measuring the terminal complement complex. Neutrophil oxidative burst and changes in CD11b and L-selectin expression were measured by flow cytometry. Complement was inhibited using the MAb 166-32 and 137-26, which block factor D and neutralize C5a, respectively. Meconium markedly activated the neutrophils, as revealed by up-regulation of CD11b, accentuation of L-selectin shedding, and induction of oxidative burst. Complement inhibition using the anti-factor D antibody completely (95-100%) blocked meconium-induced changes in CD11b and L-selectin expression, whereas oxidative burst was reduced by 60 -70%. The anti-C5a antibody inhibited the neutrophil activation to the same extent as anti-factor D. The data suggest that complement activation is largely responsible for the neutrophil inflammatory responses induced by meconium in vitro and that C5a is a key mediator of this response. Abbreviations ARDS, acute respiratory distress syndrome AU, arbitrary units DHR, dihydrorhodamine LPS, lipopolysaccharide MAS, meconium aspiration syndrome MFI, median fluorescence intensity PE, phycoerythrin PMA, phorbol-12-␤-myristat-13-␣-acetate TCC, terminal SC5b-9 complement complex Meconium aspiration syndrome (MAS) may cause a profound lung inflammation similar to acute respiratory distress syndrome (ARDS). A substantial increase in neutrophils in the airways; increased levels of inflammatory cytokines, eicosanoids, superoxide anions, and endothelin-1; expression of inducible nitric oxide synthase and cyclooxygenase-2; and activation of nuclear factor-B have been described in MAS (1-8). A profound inflammatory response and the release of leukocyte cytotoxic products have an important role in initiation and propagation of lung injury in ARDS, in which neutrophils and their cytotoxic products play a crucial role (9).The complement system is a key mediator of inflammation. Complement-mediated activation of neutrophils and monocytes leads to cytokine production; release of lipid mediators and histamine; oxidative burst; and altered expression of adhesion molecules, including increased expression of CD11b and shedding, revealed as decreased expression of CD62L. We showed recently that meconium is a potent activator of the alternative complement pathway in vitro (10). To study the interaction between all participating inflammatory systems, we used an in vitro human whole-blood model that is based on the use of lepirudin, a thrombin-specific anticoagulant that does not interfere with complement activation (11). We hypot...

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“…resulting in the induction of anaphylactoid shock. [24][25][26][27][28] The lethal toxicity of CAWS 8) and O9 LPS [29][30][31] is similar with respect to the following. 1) Lethal toxicity occurs 15-60 min after intravenous injection.…”

Section: )mentioning

confidence: 98%

Candida albicans Derived Fungal PAMPS, CAWS, Water Soluble Mannoprotein-.BETA.-Glucan Complex Shows Similar Immunotoxicological Activity with Bacterial Endotoxin from Escherichia coli O9

Tada

Nagi-Miura

Adachi

et al. 2006

Biological & Pharmaceutical Bulletin

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Shock is a serious clinical problem because of high mortality. There are many mechanisms inducing shock and major mechanisms related to immune dysfunction are anaphylaxis, septic shock, and endotoxin shock. Shock is usually difficulty to treat, because it is a systemic response involving not only changes in immunological parameters but inducing dysfunction of circulation, coagulation and fibrinolysis. 1) There have been many studies establishing and analyzing animal models of shock. We have also long been analyzing septic and endotoxic shock from various points of view such as, the detoxification of endotoxin by lysozyme, modulation of antibiotic action by lysozyme, 2,3) development of a monoclonal anti-CD14 antibody and its application, 4,5) and establishing an endogenous septic shock model using non-steroidal anti-inflammatory drugs. 6,7) In the course of studying early diagnosis of deep seated fungal infection we have found a limulus factor G activating activity in a water soluble polysaccharide fraction rich in mannan, named Candida albicans water soluble fraction (CAWS), released from Candida albicans, and it strongly caused acute anaphylaxis-like shock in mice. 8)The pathogenic yeast Candida albicans, a commensal of the human digestive tract and vaginal mucosa, is now one of the most common microbes of bloodstream infections in immunocompromised or intensive-care patients.9) The invasive mycoses including candidiasis, aspergillosis and cryptococcosis are increasingly becoming associated with immunosuppressive therapies and immunodeficiency associated with infections of the human immunodeficiency virus. The associated crude mortality is extensively high (38 to 75%), despite appropriate treatment with anti-fungal drugs.10-13) Sepsis, which is caused by a Gram-negative bacterial infection, has also increased for the reasons described above and the associated mortality is markedly high. 14)We previously obtained a water-soluble fraction (CAWS), prepared from the culture supernatants of Candida albicans grown in a completely synthetic medium. CAWS is mainly composed of a complex of mannoprotein and b-1,3-, b-1,6-glucans.15,16) CAWS exhibits various potential biological activities, such as cytokine synthesis by leukocytes, platelet aggregation, lethal toxicity like anaphylactoid shock, induction of coronary arteritis in various strains of mice, and so on. [17][18][19][20] However, the detailed mechanisms of these biological activities are unclear.It is reported that the intravenous injection of lipopolysaccharide from Escherichia coli O9, which possesses the mannose homopolysaccharide (MHP) as the O-antigen region, induced anaphylactoid shock within 15-60 min, but not lipopolysaccharide (LPS) from Escherichia coli O111, which possesses a heterosaccharide (not containing mannose). 21,22) The characteristics of this shock differ from those of the well-known endotoxic shock with respect to time until shock occurs and can be evoked in LPS-hyposensitive mice, like C3H/HeJ strain, 23) with a defect in Toll-like recept...

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Role of the complement‐lectin pathway in anaphylactoid reaction induced with lipopolysaccharide in mice

Cited by 16 publications

References 38 publications

Interaction of human mannose-binding lectin (MBL) with Yersinia enterocolitica lipopolysaccharide

Interaction of human mannose-binding lectin (MBL) with Yersinia enterocolitica lipopolysaccharide

Complement C5a Is a Key Mediator of Meconium-Induced Neutrophil Activation

Candida albicans Derived Fungal PAMPS, CAWS, Water Soluble Mannoprotein-.BETA.-Glucan Complex Shows Similar Immunotoxicological Activity with Bacterial Endotoxin from Escherichia coli O9

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